Evidence map›Paper›PMID 18676849›Full record

ArticleCancer research2008

Effect of ablation or inhibition of stromal matrix metalloproteinase-9 on lung metastasis in a breast cancer model is dependent on genetic background.

Michelle D Martin, Kathy J Carter, Sharon R Jean-Philippe, Mayland Chang, Shahriar Mobashery, Sophie Thiolloy, Conor C Lynch, Lynn M Matrisian, Barbara Fingleton

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  12. Review
  13. Metabolism of the Selective Matrix Metalloproteinase-9 Inhibitor (ACS pharmacology & translational science · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Development of a novel murine model of lymphatic metastasis.Clinical & experimental metastasis · 2020
    Article
  18. Article
  19. Article
  20. Article

17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Michelle D MartinDepartment of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-6840, USA.
Kathy J Carter
Sharon R Jean-Philippe
Mayland Chang
Shahriar Mobashery
Sophie Thiolloy
Conor C Lynch
Lynn M Matrisian
Barbara Fingleton
University of Notre Dame · USVanderbilt University Medical Center · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Tumor and Stromal Metalloproteinases in Breast CancerR01CA084360 · NCI · VANDERBILT UNIVERSITY · PI FINGLETON, BARBARA · 2000 to 2014
$5.7M
Intervention of Disease by Selective Gelatinase InhibitorsR01CA122417 · NCI · UNIVERSITY OF NOTRE DAME · PI CHANG, MAYLAND F, MOBASHERY, SHAHRIAR · 2007 to 2011
$1.9M
NCI NIH HHS P30 CA068485NCI NIH HHS R01 CA084360NCI NIH HHS R01 CA122417NCI NIH HHS R01CA122417NCI NIH HHS R01CA84360
6 · The paper itself

Abstract

Matrix metalloproteinases (MMP) are a family of enzymes with a myriad of functions. Lately, we have come to realize that broad-spectrum inhibition of these enzymes, as was tried unsuccessfully in multiple phase III trials in cancer patients, is likely unwise given the protumorigenic and antitumorigenic functions of various family members. Here, we used the multistage mammary tumor model MMTV-PyVT to investigate roles for either MMP7 or MMP9 in tumor progression. We found no effect of genetic ablation of MMP7 or MMP9 on the multifocal tumors that developed in the mammary glands. Lack of MMP7 also had no effect on the development of lung metastases, suggesting that MMP7 is irrelevant in this model. In contrast, MMP9 deficiency was associated with an 80% decrease in lung tumor burden. The predominant cellular source of MMP9 was myeloid cells, with neutrophils being the largest contributor in tumor-bearing lungs. Experimental metastasis assays corroborated the role of host-derived MMP9 in lung metastasis and also facilitated determination of a time frame most relevant for the MMP9-mediated effect. The lung tumors from MMP9-deficient mice showed decreased angiogenesis. Surprisingly, the antimetastatic outcome of MMP9 ablation seemed to be dependent on strain. Only mice that had genetic background derived from C57BL/6 showed reduced metastasis, whereas mice fully of the FVB/N background showed no significant effect. These strain-specific responses were also observed in a study using a highly selective pharmacologic inhibitor of MMP9 and thus suggest that responses to MMP inhibition are controlled by genetic differences.

Indexed as

Matrix Metalloproteinase InhibitorsAnimalsFemaleLung NeoplasmsMaleMammary Neoplasms, ExperimentalMatrix Metalloproteinase 9MiceMice, Inbred C57BLProtease InhibitorsStromal CellsMatrix Metalloproteinase 9Matrix Metalloproteinase InhibitorsProtease Inhibitors

Identifiers

PMID18676849
PMCPMC2789265
OpenAlexW1987245481

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.